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Syncope in a Woman Returning From a Long Flight

Educational Objective
Based on this clinical scenario and the accompanying image, understand how to arrive at a correct diagnosis.
1 Credit CME

A 58-year-old woman with no relevant medical history presented to the emergency department with syncope. Following a long flight 6 weeks prior, she had developed left calf tightness and pain, followed by shortness of breath for 1 week and then a syncopal event the day of admission. On physical examination, she appeared anxious, with a temperature of 36.8°C, a heart rate of 102 beats/minute, blood pressure of 128/66 mm Hg, a respiratory rate of 20 breaths/minute, and pulse oximetry of 98% on room air. Her heart and lung sounds were normal. Her laboratory results were notable for a troponin level of 0.07 ng/mL (to convert to μg/L, multiply by 1.0), and a fibrin D-dimer level of more than 2000 μg/mL (to convert nmol/L, multiply by 5.476). Her electrocardiogram on presentation showed sinus tachycardia and was otherwise normal. Computed tomography of the chest was performed, which showed multiple large bilateral pulmonary emboli (Figure, A), with deviation of the interventricular septum toward the left ventricle. Echocardiography demonstrated a large mobile thrombus extending from the right atrium into the right ventricle, as well as a clot in the left atrium and left ventricle that appeared to originate from the interatrial septum, suggesting a defect there (Video, Figure, B).

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Pulmonary embolism with patent foramen ovale and impending paradoxical embolism

C. Consult cardiothoracic surgery for controlled operative thrombectomy

Pulmonary embolus (PE) is a form of venous thromboembolism that accounts for approximately 100 000 deaths annually in the United States.1 Pulmonary emboli may be classified by severity into massive (PE causing hemodynamic compromise), submassive (PE causing right ventricular dysfunction), and nonmassive or low-risk PE, with 90-day mortality rates ranging from 58.3% for massive PE to less than 2% in low-risk PE.2 Clinical features suggestive of a poor prognosis include an elevated troponin or natriuretic peptide level, right-to-left ventricular septal bowing or right ventricular enlargement on computed tomography, and right ventricular dysfunction on echocardiography, all of which were evident in this patient.3 Treatment approaches vary by the severity of PE. Therapeutic anticoagulation with unfractionated heparin (choice A), low-molecular-weight heparin, or a direct oral anticoagulant is recommended for all acute PE, with no absolute contraindications to anticoagulation. The management of submassive and massive PEs is more complex. For patients with massive or otherwise high-risk PEs, such as this patient, the American Heart Association suggests fibrinolysis (choice D) if there is acceptably low risk of bleeding complications.4 However, either catheter embolectomy and fragmentation (choice B) or surgical embolectomy (choice C) is reasonable if fibrinolysis is contraindicated or patients remain unstable after fibrinolysis.4

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Article Information

Corresponding Author: Monica M. Parks, MD, Department of Medicine, University of California, San Francisco, PO Box 0119, 505 Parnassus Ave, Room 987, San Francisco, CA 94143 (monica.parks@ucsf.edu).

Published Online: February 19, 2020. doi:10.1001/jamacardio.2019.5452

Conflict of Interest Disclosures: None reported.

Additional Contributions: We thank the patient for granting permission to publish this information.

References
1.
Office of the Surgeon General (US); National Heart, Lung, and Blood Institute (US).  The Surgeon General's Call to Action to Prevent Deep Vein Thrombosis and Pulmonary Embolism. Rockville, MD: Office of the Surgeon General (US); 2008.
2.
Bova  C, Pesavento  R, Marchiori  A,  et al; TELESIO Study Group.  Risk stratification and outcomes in hemodynamically stable patients with acute pulmonary embolism: a prospective, multicentre, cohort study with three months of follow-up.  J Thromb Haemost. 2009;7(6):938-944. doi:10.1111/j.1538-7836.2009.03345.xPubMedGoogle ScholarCrossref
3.
Aggarwal  V, Nicolais  C, Lee  A, Bashir  R. Acute management of pulmonary embolism. https://www.acc.org/latest-in-cardiology/articles/2017/10/23/12/12/acute-management-of-pulmonary-embolism. Published October 24, 2017. Accessed April 23, 2019.
4.
Jaff  MR, McMurtry  MS, Archer  SL,  et al; American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology.  Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association.  Circulation. 2011;123(16):1788-1830. doi:10.1161/CIR.0b013e318214914fPubMedGoogle ScholarCrossref
5.
Hagen  PT, Scholz  DG, Edwards  WD.  Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts.  Mayo Clin Proc. 1984;59(1):17-20. doi:10.1016/S0025-6196(12)60336-XPubMedGoogle ScholarCrossref
6.
Homma  S, Sacco  RL, Di Tullio  MR, Sciacca  RR, Mohr  JP; PFO in Cryptogenic Stroke Study (PICSS) Investigators.  Effect of medical treatment in stroke patients with patent foramen ovale: patent foramen ovale in Cryptogenic Stroke Study.  Circulation. 2002;105(22):2625-2631. doi:10.1161/01.CIR.0000017498.88393.44PubMedGoogle ScholarCrossref
7.
Podroužková  H, Horváth  V, Hlinomaz  O,  et al.  Embolus entrapped in patent foramen ovale: impending paradoxical embolism.  Ann Thorac Surg. 2014;98(6):e151-e152. doi:10.1016/j.athoracsur.2014.08.072PubMedGoogle ScholarCrossref
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